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Purpose Personality traits, such as dispositional optimism and pessimism, have impact on a variety of health-related problems. Influence on outcome in total knee arthroplasty (TKA) could only be shown for other personality trait concepts, but not for dispositional optimism/pessimism. This study aims to examine the association of dispositional optimism/pessimism with pre-operative joint function and post-operative outcome in TKA. Methods Data were acquired in a multicentre, cross-sectoral, prospective study (the PROMISE Trial). Patients were followed for 12 months post-operatively. Dispositional optimism/pessimism was measured pre-operatively via the revised Life Orientation Test (LOT-R), pre- and post-operative function was measured via the 12 Item Knee-osteoarthritis outcome Scores (KOOS-12). Log-linear regression models considering known confounders and t-test were carried out to show the association of LOT-R scores with pre- and post-operative KOOS-12 scores. Results 740 patients were analyzed. Optimistic LOT-R was significantly positively associated to the mean scores of KOOS-12 pre- and post-operative, while pessimistic LOT-R was significantly associated negatively (pre-operative: optimistic p = 0.001, pessimistic p = 0.001; post-operative optimistic: 3M p = 0.001, 6M p = 0.001, 12M p = 0.001; post-operative pessimistic: 3M p = 0.01, 6M p = 0.004, 12M p = 0.001). Conclusion Optimism was positively associated with pre-operative joint function and, more importantly, post-operative functional outcome in TKA, while pessimism was associated with the opposite. Assessing patients’ general personality traits prior to surgery to identify pessimistic patients, hence being at risk for poor outcome in TKA, should be considered to react to the patients’ special needs and possible pessimistic expectations, i.e., through a cognitive–behavioral intervention, to potentially increase optimism and hereby post-operative outcome in TKA. Level of evidence Prognostic Level III.

Background Symptoms of depersonalization (DP) and derealization (DR) have a high prevalence in patient and community samples. Previous studies suggested that DP/DR symptoms might represent a marker of disease severity and poor prognosis. However, population-based studies investigating the impact of DP/DR symptoms on the course of depression and anxiety are sparse. Therefore, we aimed to analyze whether symptoms of DP/DR are longitudinally associated with the persistence or incidence of elevated symptoms of depression/anxiety. Methods We analyzed observational data from a sample of 13.182 participants of the Gutenberg Health Study. The outcomes were elevated symptoms of depression/anxiety at the 2.5 years follow-up as determined by the 2-item depression scale (PHQ-2), the 2-item anxiety scale (GAD-2), and the compound measure PHQ-4 respectively. The predictor was the 2-item Cambridge Depersonalization Scale (CDS-2). Results 8.7% of the sample were bothered by symptoms of DP/DR at baseline. They had an increased risk for elevated symptoms of depression/anxiety at the 2.5-year follow-up beyond baseline depression/anxiety and other factors. Each point increment in the CDS-2 scale, ranging from 0-6, was associated with a 21% increase of risk for PHQ-4 ≥ 3 at the follow-up (odds ratio 1.21, 95% confidence interval 1.11-1.32). Limitations The study was mostly questionnaire-based. Conclusion Symptoms of DP/DR are independent risk factors for the persistence or incidence of elevated symptoms of depression/anxiety. Symptoms of DP/DR represent an easily assessable risk factor for the course of mental disorders. Treatment and prevention of mental disorders might benefit from the broader recognition of these phenomena.

Introduction: Depression and cardiovascular disease represent two of the most common causes of disability and mortality. In patients with heart failure (HF), depressive symptoms are related to worse outcomes. Reduced heart rate variability (HRV), as a marker for cardiac autonomic dysfunction, is proposed to mediate the relation between depressive symptoms and cardiovascular health. Hypothesis: This explorative study aims to identify HRV parameters that are related to the somatic-affective and cognitive-affective dimension of depression in subjects with HF, separatly for HF with reduced (HFrEF; EF < 50 %) and preserved ejection fraction (HFpEF; EF > 50%). Methods: We examined the association between depressiveness as assessed by the Patient-Health-Questionnaire-9 (PHQ-9) and HRV parameters from 24h-Holter ECG recording in the MyoVasc study (NCT04064450; N=3,289), a prospective cohort study on chronic HF. HRV parameters related to PHQ-9 have been selected via elastic net regression. Multivariable linear regression analysis adjusted for age, sex, established cardiovascular risk factors, comorbidities, medication and NTpro-BNP has been performed. Results: In the analysis sample (HRV analysis in N=1,001), 29.8% had mild depressive symptoms (PHQ-9 = 5-9) and 10.2% had major depressive symptoms (PHQ-9 ≥ 10). Elastic net selected 10 HRV parameters. The severity of depression according to PHQ-9 sum scores correlated with triangular index (HRVi) (coefficient estimate (β)) = -0.02, 95% CI: -0.04, -0.006, p = 0.01), acceleration capacity (β = 0.021, 95% CI: 0.004, -0.04, p = 0.02), deceleration capacity (β = -0.02, 95% CI: -0.04, -0.003, p = 0.02), IRRR (β = -0.02, 95% CI: -0.04, -0.003, p = 0.02), SDANN (β = -0.02, 95% CI: -0.04, -0.004, p=0.02) and ULF (β = -0.03, 95% CI: -0.05, -0.01, p = 0.002). Cognitive dimension of depression correlated with HRVi in subjects with HFrEF (β = -0.08, 95% CI: -0.15, -0.008, p = 0.03). Somatic dimension of depression correlated with acceleration capacity in HFpEF (β = 0.06, 95% CI: 0.0025, 0.11, p = 0.04). Conclusions: HRV parameters were consistently more reduced in individuals with more depressive symptoms. Interestingly, HRV parameters differ regarding the cognitive and somatic dimension of depression in individuals with HF.

Etwa 20–50 % der Patienten mit einem akuten Koronarsyndrom erleben zusatzlich zum akuten Brustschmerz Todesangst. Diese umfasst Symptome, die viele Patienten auch im weiteren Verlauf nicht mehr loslassen. Todesangst und Brustschmerzen sind deshalb wichtige Themen fur die Psychotherapie von Herzpatienten. Empirische Untersuchungen zur Bedeutung der Todesangst erbrachten sehr widerspruchliche Befunde: Todesangst war einerseits deutlich mit einer starkeren psychischen Belastung assoziiert, andererseits aber auch mit einer wesentlich besseren Prognose. Fur die Aufklarung dieses Widerspruchs ist ein affektfokussierter Untersuchungs- und Behandlungsansatz hilfreich. Todesangst als Reaktion auf eine lebensbedrohliche Situation ist hochgradig adaptiv und Zeichen einer gesunden Selbstfursorge. In anderen Fallen allerdings ist Todesangst keine adaptive emotionale Reaktion, sondern Ausdruck maladaptiver Abwehrmechanismen wie beispielsweise im Rahmen einer somatischen Belastungsstorung (nach DSM-5): Somatisierung der Angst in Form von Brustschmerzen und anhaltend unangemessene Angste und Sorgen wegen der korperlichen Symptome. Die affektfokussierte Exploration erlaubt diese Differenzierung und ermoglicht es dem Patienten, diese Unterschiede nachzuvollziehen und adaptive Verhaltensweisen aufzubauen.

Background Socioeconomic status (SES) has a strong association with depression or physical and mental health in general. However, as SES is a multifaceted construct these associations are not easy to explain. Further, there are several indicators and many studies only investigating two or less indicators at the same time. Therefore, this study aims to analyze the cross-sectional and longitudinal association of three defined SES dimensions (education, occupational position and household net-income) with the occurrence of elevated symptoms of depression relative to the impact of important covariates. Methods The study included observational data from 12,484 participants of the Gutenberg Health Study. The outcome was “elevated depressive symptoms” as defined by Patient Health Questionnaire (PHQ-2) ≥ 2 at the 2.5-year follow-up. Regression coefficients were adjusted for baseline covariates (age, sex, partnership, depression, anxiety, medical history of depressive or anxiety disorder and major medical diseases (MMD)) in addition to SES sum score and the three single indicators. We further examined interaction terms of the SES with sex, partnership and major medical diseases. We analyzed the sample stratified by elevated depressive symptoms at baseline, as we expected different trajectories in both subgroups. Results SES, education and household net-income were lower in the group of persons with PHQ-2 ≥ 2 at baseline, and they predicted the occurrence of PHQ-2 ≥ 2 at 2.5 year follow-up in the group of persons without elevated depressive symptoms at baseline after multivariable adjustment (SES: Odds Ratio (OR) 0.96, 0.95–0.98, p

Psychosocial stress has a profound impact on well-being and health. The response to stress is associated mainly with the amygdala, a crucial structure of the fear-defense system, essential for social cognition and emotion regulation. Recent neuroimaging-studies demonstrated how an increased metabolic activity of the amygdala enhances inflammation, and leads to cardiometabolic disease. The development of therapeutic strategies depends on our understanding of both which factors activate the fear-defense system and the subsequent molecular mechanisms that translate emotional stress into cell damage. Fear of emotions as an aftermath of attachment trauma is the most important trigger of the maladaptive activation of the fear-defense system. The central molecular pathways are enhanced myelopoiesis and upregulated proinflammatory gene expression, glucocorticoid and insulin resistance, and oxidative stress. Therapeutic strategies may benefit from holistic approaches. Psychotherapy can reduce the maladaptively increased activation of the fear-defense system. Biological interventions can buffer the detrimental effects of oxidative stress in the organism., Highlights • The maladaptive activation of the fear-defense system is an essential contributor to inflammation and oxidative stress. • Fear of emotions as an aftermath of attachment trauma is the most important trigger that activates the fear-defense system. • Mental disorders are associated with reduced life expectancy due to increased oxidative stress. • Treatment of oxidative stress should involve pharmacological approaches, and psychological interventions.

BackgroundBased on the vulnerability–stress model, we aimed to (1) determine new onset of depression in individuals who had not shown evidence of depression at baseline (5 years earlier) and (2) identify social, psychological, behavioral, and somatic predictors.MethodsLongitudinal data ofN= 10 036 participants (40–79 years) were evaluated who had no evidence of depression at baseline based on Patient Health Questionnaire (PHQ-9), no history of depression, or intake of antidepressants. Multivariate logistic regression models were used to predict the onset of depression.ResultsPrevalence of new cases of depression was 4.4%. Higher rates of women (5.1%) than men (3.8%) were due to their excess incidence ConclusionsPsychobiological vulnerability, stress, and illness-related factors were predictive of new onset of depression, whereas social support was protective. Baseline subclinical depression was an additional risk weakening the relationship between anxiety and depression by taking their overlap into account. Vulnerability factors differed between men and women.

Erratum zu: Psychotherapeut 2017 https://doi.org/10.1007/s00278-017-0247-z Im Originalbeitrag wurde der Name der Autorin Jasmin Ghaemi Kerahrodi nicht korrekt aufgefuhrt. Bitte beachten Sie, dass der Vorname der Autorin „Jasmin“ lautet, der Nachname „Ghaemi Kerahrodi“. Die korrekte Zitierweise des …

Objective— Peroxisome proliferator-activated receptor γ, coactivator 1α (PGC-1α) is an important mediator of mitochondrial biogenesis and function. Because dysfunctional mitochondria might be involved in the pathogenesis of vascular disease, the current study was designed to investigate the effects of in vivo PGC-1α deficiency during chronic angiotensin II (ATII) treatment. Approach and Results— Although ATII infusion at subpressor doses (0.1 mg/kg per day for 7 days) did not cause vascular dysfunction in wild-type mice, it led to impaired endothelial-dependent and endothelial-independent relaxation in PGC-1α knockout mice. In parallel, oxidative stress was increased in aortic rings from ATII-treated PGC-1α knockout mice, whereas no change in nitric oxide production was observed. By using the mitochondrial-specific superoxide dye MitoSox and complex I inhibitor rotenone, we identified the mitochondrial respiratory chain as the major PGC-1α–dependent reactive oxygen species source in vivo, accompanied by increased vascular inflammation and cell senescence. In vivo treatment with the mitochondria-targeted antioxidant Mito-TEMPO partially corrected endothelial dysfunction and prevented vascular inflammation in ATII-treated PGC-1α mice, suggesting a causative role of mitochondrial reactive oxygen species in this setting. Conclusions— PGC-1α deletion induces vascular dysfunction and inflammation during chronic ATII infusion by increasing mitochondrial reactive oxygen species production.

CD40 ligand (CD40L) is involved in the vascular infiltration of immune cells and pathogenesis of atherosclerosis. Additionally, T cell CD40L release causes platelet, dendritic cell and monocyte activation in thrombosis. However, the role of CD40L in angiotensin II (ATII)-driven vascular dysfunction and hypertension remains incompletely understood. We tested the hypothesis that CD40L contributes to ATII-driven vascular inflammation by promoting platelet-leukocyte activation, vascular infiltration of immune cells and by amplifying oxidative stress. C57BL/6 and CD40L-/- mice were infused with ATII (1 mg/kg/day for 7 days) using osmotic minipumps. Vascular function was recorded by isometric tension studies, and reactive oxygen species (ROS) were monitored in blood and heart by optical methods. Western blot, immunohistochemistry, FACS analysis and real-time RT-PCR were used to analyze immune cell distribution, pro-inflammatory cytokines, NAPDH oxidase subunits, T cell transcription factors and other genes of interest. ATII-treated CD40L-/- mice showed improved endothelial function, suppression of blood platelet-monocyte interaction (FACS), platelet thrombin generation (calibrated automated thrombography) and coagulation (bleeding time), as well as decreased oxidative stress in the aorta, heart and blood compared to wild-type mice. Moreover, ATII-treated CD40L-/- mice displayed decreased levels of TH1 cytokines released by splenic CD4⁺ T cells (ELISA) and lower expression levels of NOX-2, T-bet and P-selectin as well as diminished immune cell infiltration in aortic tissue compared to controls. Our results demonstrate that many ATII-induced effects on vascular dysfunction, such as vascular inflammation, oxidative stress and a pro-thrombotic state, are mediated at least in part via CD40L.

Our previous studies identified potent antioxidant effects and improvement of vascular function by telmisartan therapy in experimental diabetes and nitrate tolerance. The present study compared the beneficial effects of single telmisartan or amlodipine versus telmisartan/amlodipine combination therapy (T+A) in streptozotocin (STZ)-induced type 1 diabetic rats. Male Wistar rats were injected once with STZ (60 mg/kg, i.v.) and 1 week later the drugs (telmisartan, amlodipine, or T+A) were administrated orally by a special diet (2.5-5 mg kg(-1) day(-1)) for another 7 weeks. We only observed a marginal beneficial on-top effect of T+A therapy over the single drug regimen that was most evident in the improvement of endothelial function (acetylcholine response) and less pronounced in the reduction of whole blood, vascular and cardiac oxidative stress (blood leukocyte oxidative burst, aortic dihydroethidine and 3-nitrotyrosine staining, as well as cardiac NADPH oxidase activity and uncoupling of endothelial nitric oxide synthase) in diabetic rats. These effects on oxidative stress parameters were paralleled by those on the expression pattern of NADPH oxidase and nitric oxide synthase isoforms. In addition, development of mild hypotension in the T+A-treated rats was observed. Reasons for this moderate synergistic effect of T+A therapy may be related to the potent beneficial effects of telmisartan alone and the fact that amlodipine and telmisartan share similar pathways to improve endothelial function. Moreover, hypotension in the T+A-treated rats could partially antagonize the beneficial additive effects by counter-regulatory mechanisms (e.g., activation of the renin-angiotensin-aldosterone system).